White certain host-related and environmental causes of human oral candidiasis have been well-documented (tetracycline therapy, steroids, lymphocyte deficits), frequently the disease occurs for no apparent reason. We have demonstrated, using the model for chronic oral candidiasis in the rat, that various strains of Candida albicans have differing abilities to infect rat lingual mucosa. These strain-related differences in mucosal pathogenicity may, in part, account for the wide clinical spectrum of candidiasis, and it may be that those episodes of candidiasis which develop in otherwise normal patients represent infection by a more pathogenic strain of yeast. The purpose of this investigation would be to more fully characterize the rat mucosal pathogenicity of C. albicans isolates and possibly correlate this pathogenicity with the severity of the human lesions from which they were isolated. This would involve the identification of mucosally pathogenic strains. The development of the rat tongue lesions induced by this organism would be examined temporally by means of gross, light microscopic, and SEM observations. Comparisons would be made between the less pathogenic and more pathogenic strains. An attempt will be made to increase the musocal pathogenicity of a strain of C. albicans which currently produces lesions in 80% of inoculated rats.